Brown Fat and Obesity: The Next Big Thing?

Mark Stephens, Marian Ludgate; D. Aled Rees


Clin Endocrinol. 2011;74(6):661-670. 

In This Article

Energy Balance and Thermogenesis

Obesity is the product of a mismatch in energy supply and utilization, resulting in the deposition of WAT. In humans, this is almost inevitably because of a combination of excessive dietary intake and too little exercise. Interestingly, excision or denervation of BAT in animal models leads to an abnormal increase in WAT,[1] implying a significant impact upon energy balance. The primary function of BAT is in the generation of heat. Thermogenic mechanisms are customarily classified as either obligatory or facultative. Obligatory thermogenesis (OT) represents the energy dissipated as heat in the many energetic transformations inherent in life and equates to basal metabolic rate at thermoneutrality. In a cold environment, facultative thermogenesis (FT) may be required to maintain core temperature. Initially, heat is produced by shivering, which is replaced as acclimatization proceeds with nonshivering mechanisms in which BAT activation plays a key role. In small mammals, cold-induced thermogenesis in the absence of shivering accounts for an average of 11·8% of the resting metabolic rate, with high individual variation.[3] Some observations have indicated that food intake results in a similar activation of brown adipocytes,[4] which has been taken as evidence in support of diet-induced thermogenesis. This envisages BAT acting not only to maintain body temperature but as a protector against obesity in times of positive energy balance, burning off excess calories in a co-ordinated mechanism to maintain energy homeostasis. It is difficult to envisage the evolutionary drive for such a mechanism, whilst the most recent review expresses grave doubts about the existence of any such system.[5]


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